title: Characterization of the basal core promoter and precore regions in anti-HBe-positive inactive carriers of hepatitis B virus.
abstract: BACKGROUND
  The study of hepatitis B virus (HBV) genomic heterogeneity has become a major issue in investigations aimed at understanding the relationship between HBV mutants and the wide spectrum of clinical and pathological conditions associated with HBV infection. Although most chronically infected HBV patients are inactive carriers, several virological aspects of this state remain unclear.
  
  
  METHODS
  In order to determine the prevalence and clinical significance of mutations in the basal core promoter (BCP) and precore (pC) regions among inactive carriers, the nucleotide sequences from 41 inactive carriers were analyzed and compared with those from 29 individuals with chronic active hepatitis.
  
  
  RESULTS
  Genotypes A (24.3%), D (37.1%), F1b (12.9%), and F4 (18.6%) were the most prevalent. Mutations in the BCP/pC regions were observed in most of the inactive carriers (92.7%) and in most of the patients with chronic active hepatitis (93.1%). The prevalence of mutation 1764(A) was significantly higher in patients with chronic active hepatitis (65.5%) than in inactive carriers (36.6%) (p=0.038), whereas the prevalences of mutations at the other positions analyzed were not significantly different. Older patients (>50 years) showed BCP/pC patterns with a higher number of substitutions. Mutations were found to be biased by genotype: the 1896(A) mutation was highly prevalent in genotypes D and F4, while alternative substitutions in the pC region were more prevalent in genotypes A and F1b.
  
  
  CONCLUSIONS
  Mutations in the BCP/pC regions are the hallmark of chronic anti-HBe-positive individuals; nevertheless, the even distribution of mutations in active and inactive carriers suggests that BCP/pC mutations may occur during HBV infection not strictly related to the HBV infection activity.
authors.affiliation: Cátedra de Virología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, 1113 Buenos Aires, Argentina.
authors.forename: María Mora González López
authors.initials: MM
authors.lastname: Ledesma
authors.forename: Omar
authors.initials: O
authors.lastname: Galdame
authors.forename: Belén
authors.initials: B
authors.lastname: Bouzas
authors.forename: Luciana
authors.initials: L
authors.lastname: Tadey
authors.forename: Beatriz
authors.initials: B
authors.lastname: Livellara
authors.forename: Silvina
authors.initials: S
authors.lastname: Giuliano
authors.forename: Marcela
authors.initials: M
authors.lastname: Viaut
authors.forename: Silvia
authors.initials: S
authors.lastname: Paz
authors.forename: Hugo
authors.initials: H
authors.lastname: Fainboim
authors.forename: Adrian
authors.initials: A
authors.lastname: Gadano
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Campos
authors.forename: Diego
authors.initials: D
authors.lastname: Flichman
mesh_terms: D000328:Adult; D000368:Aged; D001483:Base Sequence; D002353:Carrier State / Q000453:epidemiology / Q000821:virology*; D004279:DNA, Viral / Q000097:blood / Q000302:isolation & purification; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006510:Hepatitis B Antibodies / Q000097:blood; D006513:Hepatitis B e Antigens / Q000235:genetics* / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics* / Q000472:pathogenicity; D019694:Hepatitis B, Chronic / Q000453:epidemiology / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D009154:Mutation; D010802:Phylogeny; D016133:Polymerase Chain Reaction; D011401:Promoter Regions, Genetic / Q000235:genetics*; D017422:Sequence Analysis, DNA; D013223:Statistics as Topic
chemical_list: D004279:DNA, Viral; D006510:Hepatitis B Antibodies; D006513:Hepatitis B e Antigens